Background:
The effects of exercise on the innate/inflammatory immune responses are
crucially mediated by catecholamines and adrenoreceptors; and mediations in both stimulatory and
anti-inflammatory responses have been attributed to them. Obesity and metabolic syndrome are included
among low-grade chronic inflammatory pathologies; particularly because patients have a dysregulation
of the inflammatory and stress responses, which can lead to high levels of inflammatory
cytokines that induce insulin resistance, contributing to the onset or exacerbation of type 2 diabetes.
Macrophages play a crucial role in this obesity-induced inflammation. Although most of the antiinflammatory
effects of catecholamines are mediated by β adrenergic receptors (particularly β2), it is
not known whether in altered homeostatic conditions, such as obesity and during exercise, innate/
inflammatory responses of macrophages to β2 adrenergic stimulation are similar to those in cells
of healthy organisms at baseline.
Objective:
This review aims to emphasize that there could be possible different responses to β2 adrenergic
stimulation in obesity, and exercise in this condition.
Methods:
A revision of the literature based on the hypothesis that obesity affects β2 adrenergic regulation
of macrophage-mediated innate/inflammatory responses, as well as the effect of exercise in this
context.
Conclusion:
The inflammatory responses mediated by β2 adrenoreceptors are different in obese individuals
with altered inflammatory states at baseline compared to healthy individuals, and exercise can
also interfere with these responses. Nevertheless, it is clearly necessary to develop more studies that
contribute to widening the knowledge of the neuroimmune regulation process in obesity, particularly in
this context.
Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection
